| WB | 咨询技术 | Human,Mouse,Rat |
| IF | 咨询技术 | Human,Mouse,Rat |
| IHC | 咨询技术 | Human,Mouse,Rat |
| ICC | 技术咨询 | Human,Mouse,Rat |
| FCM | 咨询技术 | Human,Mouse,Rat |
| Elisa | 咨询技术 | Human,Mouse,Rat |
| Aliases | VAV3; FLJ40431; Guanine nucleotide exchange factor VAV3; |
| Entrez GeneID | 10451; |
| WB Predicted band size | 100kDa |
| Host/Isotype | Rabbit IgG |
| Antibody Type | Primary antibody |
| Storage | Store at 4°C short term. Aliquot and store at -20°C long term. Avoid freeze/thaw cycles. |
| Species Reactivity | Human |
| Immunogen | Peptide sequence around phosphorylation site of tyrosine 173 (E-V-Y(p)-E-D) derived from Human VAV3. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide. |
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以下是关于 VAV3 (Phospho-Tyr173) 抗体的模拟参考文献示例(注：文献为虚构，仅作格式参考，实际文献需通过学术数据库查询)：
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1. **文献名称**: *"VAV3 Phosphorylation at Tyr173 Regulates HER2-Driven Breast Cancer Metastasis"*
**作者**: Smith A, et al.
**摘要**: 研究揭示了 HER2 信号通路通过磷酸化 VAV3 的 Tyr173 位点激活其鸟苷酸交换活性，促进 RAC1 依赖性乳腺癌细胞侵袭。使用特异性 Phospho-Tyr173 抗体证实其在患者样本中的高表达与转移风险相关。
2. **文献名称**: *"Tyr173 Phosphorylation of VAV3 Modulates Prostate Cancer Cell Migration"*
**作者**: Lee B, et al.
**摘要**: 通过体外实验和 Phospho-Tyr173 抗体检测，证明生长因子刺激诱导的 VAV3 Tyr173 磷酸化增强前列腺癌细胞迁移能力，且该过程依赖 PI3K 通路调控。
3. **文献名称**: *"Role of VAV3 Phosphorylation in EGFR Signaling and Tumor Angiogenesis"*
**作者**: Chen C, et al.
**摘要**: 利用 Phospho-Tyr173 特异性抗体，发现 EGFR 激活后 VAV3 Tyr173 位点磷酸化促进内皮细胞血管生成，敲除该位点显著抑制小鼠模型中的肿瘤血管形成。
4. **文献名称**: *"Development of a Phospho-Specific Antibody for VAV3 Tyr173 and Its Application in Glioblastoma"*
**作者**: Garcia D, et al.
**摘要**: 研究报道了 Phospho-Tyr173 抗体的制备与验证，证明其在胶质母细胞瘤中特异性识别活化的 VAV3.并与患者预后不良相关。
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**建议**：实际文献需通过 **PubMed** 或 **Google Scholar** 检索关键词：
`"VAV3" AND "Phospho-Tyr173"`、`"VAV3 phosphorylation" AND "antibody"`。
部分抗体公司(如 Cell Signaling Technology)的技术文档也可能提供相关引用文献。
The VAV3 (Phospho-Tyr173) antibody detects the phosphorylated form of VAV3 at tyrosine residue 173. a post-translational modification critical for its activation and function. VAV3. a member of the VAV family of guanine nucleotide exchange factors (GEFs), plays a key role in regulating Rho GTPase signaling pathways. Phosphorylation at Tyr173. located within the acidic domain of VAV3. is induced by upstream signals such as receptor tyrosine kinases (RTKs) or Src-family kinases. This modification relieves autoinhibitory interactions, enabling VAV3 to activate Rho-family GTPases (e.g., RAC, CDC42. RHO), which govern processes like cytoskeletal reorganization, cell proliferation, and migration.
Aberrant VAV3 activation, including dysregulated phosphorylation, has been implicated in cancer progression, immune disorders, and neurological diseases. The VAV3 (Phospho-Tyr173) antibody is widely used in research to study signaling dynamics in these contexts, particularly in cell lines or tissues with hyperactive RTK or Src pathways. It aids in elucidating mechanisms of oncogenic transformation, metastasis, and therapeutic resistance. Specificity for the phosphorylated Tyr173 epitope makes it a valuable tool for assessing VAV3 activation status in Western blotting, immunoprecipitation, or immunofluorescence, providing insights into pathway activity and potential biomarkers for targeted therapies.
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